title: Evaluation of troponin T criteria for periprocedural myocardial infarction in patients with acute coronary syndromes.
abstract: In patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI), the diagnosis of periprocedural myocardial infarction is often problematic when the pre-PCI levels of cardiac troponin T (TnT) are elevated. Thus, we examined different TnT criteria for periprocedural myocardial infarction when the pre-PCI TnT levels were elevated and also the associations between the post-PCI cardiac marker levels and outcomes. We established the relation between the post-PCI creatine kinase-MB (CKMB) and TnT levels in 582 patients (315 with acute coronary syndromes and 272 with stable coronary heart disease). A post-PCI increase in the CKMB levels to 14.7 μg/L (3 × the upper reference limit [URL] in men) corresponded to a TnT of 0.23 μg/L. In the 85 patients with acute coronary syndromes and normal CKMB, but elevated post peak TnT levels before PCI (performed at a median of 5 days, interquartile range 3 to 7), the post-PCI cardiac marker increases were as follows: 21 (24.7%) with a ≥ 20% increase in TnT, 10 (11.8%) with an CKMB level >3 × URL, and 12 (14%) with an absolute TnT increase of >0.09 μg/L (p <0.005 for both). In the patients with stable coronary heart disease and post-PCI cardiac markers > 3× URL compared to those without markers elevations, the rate of freedom from death or nonfatal myocardial infarction was 88% for those with TnT elevations versus 99% (p <0.001, log-rank) and 84% for those with CKMB elevations versus 98% (p <0.001, log-rank). Of the patients with acute coronary syndromes, the post-PCI marker levels did not influence the outcomes. In conclusion, in patients with acute coronary syndromes and elevated TnT levels undergoing PCI several days later, ≥20% increases in TnT were more common than absolute increments in the TnT or CKMB levels of >3× URL. Also, periprocedural cardiac marker elevations in patients with acute coronary syndromes did not have prognostic significance.
authors.affiliation: Department of Cardiology, University of New South Wales, Sydney, New South Wales, Australia.
authors.forename: Ibrahim Meloud
authors.initials: IM
authors.lastname: Shugman
authors.forename: Patrick
authors.initials: P
authors.lastname: Diu
authors.forename: Jayesh
authors.initials: J
authors.lastname: Gohil
authors.forename: Krishna Kishor
authors.initials: KK
authors.lastname: Kadappu
authors.forename: Melissa
authors.initials: M
authors.lastname: Leung
authors.forename: Sidney
authors.initials: S
authors.lastname: Lo
authors.forename: Dominic Y
authors.initials: DY
authors.lastname: Leung
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Hopkins
authors.forename: Craig P
authors.initials: CP
authors.lastname: Juergens
authors.forename: John K
authors.initials: JK
authors.lastname: French
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000401:mortality; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D003327:Coronary Disease / Q000097:blood / Q000401:mortality; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000401:mortality / Q000628:therapy; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D011446:Prospective Studies; D018709:Statistics, Nonparametric; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D020107:Troponin T; D003402:Creatine Kinase